ArticleExperimental brain research2018
Dihydrolipoamide dehydrogenase suppression induces human tau phosphorylation by increasing whole body glucose levels in a C. elegans model of Alzheimer's Disease.
Article in Experimental brain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Role and mechanisms of cuproptosis in the pathogenesis of Wilson's disease (Review).International journal of molecular medicine · 2025Review
- Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.Aging and disease · 2025Review
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Glucose enrichment reduces lifespan and promotes tau phosphorylation in human tau-expressing C. elegans, unaffected by O-β-GlcNAcylation induction.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Exploring genetic associations and drug targets for mitochondrial proteins and schizophrenia risk.Schizophrenia (Heidelberg, Germany) · 2025Article
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- Article
- Roles of Dihydrolipoamide Dehydrogenase in Health and Disease.Antioxidants & redox signaling · 2023Review
- Systemic alterations of tricarboxylic acid cycle enzymes in Alzheimer's disease.Frontiers in neuroscience · 2023Article
- Functional Roles of UNC-13/Munc13 and UNC-18/Munc18 in Neurotransmission.Advances in neurobiology · 2023Review
- Energy Crisis Links to Autophagy and Ferroptosis in Alzheimer's Disease: Current Evidence and Future Avenues.Current neuropharmacology · 2023Article
- Cuproptosis-a potential target for the treatment of osteoporosis.Frontiers in endocrinology · 2023Review
- The pathogenesis of DLD-mediated cuproptosis induced spinal cord injury and its regulation on immune microenvironment.Frontiers in cellular neuroscience · 2023Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Neuroprotective Effects of Oligosaccharides in Rehmanniae Radix on TransgenicFrontiers in pharmacology · 2022Article
- Two years of SARS-CoV-2 infection (2019-2021): structural biology, vaccination, and current global situation.The Egyptian journal of internal medicine · 2022Review
- Suppression of a core metabolic enzyme dihydrolipoamide dehydrogenase (Genes & diseases · 2021Article
- Non-Rodent Genetic Animal Models for Studying Tauopathy: Review ofInternational journal of molecular sciences · 2021Review
- The Role of the Rare Variants in the Genes Encoding the Alpha-Ketoglutarate Dehydrogenase in Alzheimer's Disease.Life (Basel, Switzerland) · 2021Article
- Review
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microtubule associated tau protein becomes hyperphosphorylated in Alzheimer's disease (AD). While hyperphosphorylation promotes neurodegeneration, the cause and consequences of this abnormal modification are poorly understood. As impaired energy metabolism is an important hallmark of AD progression, we tested whether it could trigger phosphorylation of human tau protein in a transgenic Caenorhabditis elegans model of AD. We found that inhibition of a mitochondrial enzyme of energy metabolism, dihydrolipoamide dehydrogenase (DLD) results in elevated whole-body glucose levels as well as increased phosphorylation of tau. Hyperglycemia and tau phosphorylation were induced by either RNAi suppression of the dld-1 gene or by inhibition of the DLD enzyme by the inhibitor, 2-methoxyindole-2-carboxylic acid (MICA). Although the calcium ionophore A23187 could reduce tau phosphorylation induced by either chemical or genetic suppression of DLD, it was unable to reduce tau phosphorylation induced by hyperglycemia. While inhibition of the dld-1 gene or treatment with MICA partially reversed the inhibition of acetylcholine neurotransmission by tau, neither treatment affected tau inhibited mobility. Conclusively, any abnormalities in energy metabolism were found to significantly affect the AD disease pathology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.